Erectile dysfunction may be common among men with diabetes, but its prevalence is still debated. We aimed to assess the relative prevalence of erectile dysfunction in diabetes searching major databases from inception to November 2016 for studies reporting erectile dysfunction in men with Type 1 and Type 2 diabetes mellitus. We conducted a meta-analysis of the prevalence [and 95% confidence intervals (95% CIs)] of erectile dysfunction in diabetes compared with healthy controls, calculating the relative odds ratios (ORs) and 95% CIs. A random effect model was applied. From 3747 initial hits, 145 studies were included representing 88 577 men (age: 55.8 ± 7.9 years). The prevalence of erectile dysfunction in diabetes overall was 52.5% (95% CI, 48.8 to 56.2) after adjusting for publication bias, and 37.5%, 66.3% and 57.7% in Type 1, Type 2 and both types of diabetes, respectively (P for interaction < 0.0001). The prevalence of erectile dysfunction was highest in studies using the Sexual Health Inventory for Men (82.2%, 17 studies, P for interaction < 0.0001). Studies with a higher percentage of people with hypertension moderated our results (beta = 0.03; 95% CI, 0.008 to 0.040; P = 0.003; R = 0.00). Compared to healthy controls (n = 5385) men with diabetes (n = 863) were at increased odds of having erectile dysfunction (OR 3.62; 95% CI, 2.53 to 5.16; P < 0.0001; I = 67%, k = 8). Erectile dysfunction is common in diabetes, affecting more than half of men with the condition and with a prevalence odds of approximately 3.5 times more than controls. Our findings suggest that screening and appropriate intervention for men with erectile dysfunction is warranted.

Human papillomaviruses (HPVs) are agents of the most common sexually transmitted diseases in females and males. Precise data about the presence, mechanism of infection and clinical significance of HPV in the male reproductive tract and especially in sperm are not available. Here we show that HPV can infect human sperm, it localizes at the equatorial region of sperm head through interaction between the HPV capsid protein L1 and syndecan-1. Sperm transfected with HPV E6/E7 genes and sperm exposed to HPV L1 capsid protein are capable to penetrate the oocyte and transfer the virus into oocytes, in which viral genes are then activated and transcribed. These data show that sperm might function as vectors for HPV transfer into the oocytes, and open new perspectives on the role of HPV infection in males and are particularly intriguing in relation to assisted reproduction techniques.

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A reduction in natural and assisted cumulative pregnancy rate and an increase in miscarriage rate are related to the presence of HPV at sperm level. Although the exact mechanism by which sperm infection is able to impair fertility remains unclear, this aspect is worthy of further investigations. If confirmed, these results could change the clinical and diagnostic approach to infertile couples.

This study shows that Heparinase-III treatment seems not to affect spermatozoa in vitro and suggests that this treatment should be investigated further as a means of preparing sperm from patients who are infected with HPV in order to reduce the risk of HPV infection when using assisted reproduction techniques.

No external funding was sought for this study, and the authors have no conflict of interest to declare.

BackgroundHuman papillomavirus (HPV) currently represents an important risk factor for cancer development and infertility in humans. Whilst binding of HPV to spermatozoa has been associated with male infertility, an investigation about the presence of HPV-DNA in non-spermatozoal semen cells is lacking. Previous findings documented the presence of HPV in peripheral blood leukocytes. The aim of this study was to investigate the expression of HPV markers in semen and blood leukocytes during HPV-16 infection.MethodsA total of 32 subjects, 16 patients affected by HPV-16 semen infection and 16 controls, were evaluated in our andrological centre and enrolled in the study. Semen non-spermatozoal cells from all subjects were isolated and evaluated for the expression of HPV-16 markers (DNA and L1, E6 proteins) and further characterized for their molecular phenotype. Analogue determination was performed on peripheral blood mononuclear cells.ResultsThe presence of HPV-DNA by FISH analysis in a round cell population from semen, confirmed to be CD45+ leukocytes, was observed. These HPV-DNA containing-cells also displayed HPV-16-E6 and HPV-16-L1 viral proteins and, upon further investigation, were found to be CD20+ and CD56+, likely phenotypes of B cells and natural killer cells (NK) respectively. In 25% of the patient group, a very small population of peripheral blood mononuclear cells was found to be positive for HPV-DNA via FISH. These cells displayed the CD20+ and CD56+ phenotype alike. None of the control subjects displayed HPV-DNA in either semen or peripheral blood.ConclusionConsidering the role of CD20+ and CD56+ cell populations in the antiviral immune response, the detection of HPV markers on leukocytes may reflect the presence of virus particles within the endosomal compartment. However, the presence of HPV markers in circulating mononuclear cells raise concerns about the risk of developing cancers to distal organs.